Bertram, D. S. (1971). Mosquitoes of British Honduras, with some comments on malaria, and on arbovirus antibodies in man and equines. Trans R Soc Trop Med Hyg, 65(6), 742–762.
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Beveridge, W. I. (1993). Unravelling the ecology of influenza A virus. Hist Philos Life Sci, 15(1), 23–32.
Abstract: For 20 years after the influenza A virus was discovered in the early 1930s, it was believed to be almost exclusively a human virus. But in the 1950s closely related viruses were discovered in diseases of horses, pigs and birds. Subsequently influenza A viruses were found to occur frequently in many species of birds, particularly ducks, usually without causing disease. Researchers showed that human and animal strains can hybridise thus producing new strains. Such hybrids may be the cause of pandemics in man. Most pandemics have started in China or eastern Russia where many people are in intimate association with animals. This situation provides a breeding ground for new strains of influenza A virus.
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Birch, H. L., Bailey, A. J., & Goodship, A. E. (1998). Macroscopic 'degeneration' of equine superficial digital flexor tendon is accompanied by a change in extracellular matrix composition. Equine Vet J, 30(6), 534–539.
Abstract: Injuries to the superficial digital flexor tendon are common in horses required to gallop and jump at speed. Partial rupture of this tendon usually occurs in the central core of the midmetacarpal region and may be preceded by localised degenerative changes. Post mortem examination of apparently normal equine flexor tendons has revealed an abnormal macroscopic appearance in the central core, characterised by a reddish discolouration. We have previously shown that there is also physical damage to the collagen fibres. In the present study we tested the hypothesis that the abnormal appearance is accompanied by changes in the composition of the extracellular matrix of the tendon. Biochemical analysis of the extracellular matrix demonstrated an increase in total sulphated glycosaminoglycan content, increase in the proportion of type III collagen and decrease in collagen linked fluorescence in the central core of 'degenerated' tendons relative to tissue from the peripheral region of the same tendon. Dry matter content and total collagen content were not significantly different between tendon zones or normal and 'degenerated' tendons. These changes suggest a change in cell metabolism and matrix turnover in the central core of the tendon and are likely to contribute to a decrease in mechanical properties in this part of the tendon, predisposing to the characteristic partial rupture of the tendon.
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Blazyczek, I., Hamann, H., Deegen, E., Distl, O., & Ohnesorge, B. (2004). Retrospective analysis of 50 cases of guttural pouch tympany in foals. Vet. Rec., 154(9), 261–264.
Abstract: Between 1994 and 2001, guttural pouch tympany was diagnosed in 51 foals; there were approximately three times as many fillies as colts, of Arabian, different German warmblood breeds and Western horse breeds. There were significantly more Arabian and paint horse foals than expected in comparison with the breed distribution of the foals hospitalised at the Clinic for Horses. The foals' breed and sex did not influence the age of onset, the type and severity of the clinical signs or the recurrence rate. A surgical laser technique was used on 50 of the foals; in 35 cases only one surgical treatment was necessary, in seven cases a second operation was required during the foal's initial period of hospitalisation, and in eight cases a second operation was performed during a second period of hospitalisation. Long-term follow-up information was obtained for 44 of the 50 treated horses; 24 of them were under two years of age and 20 were over two years of age. In six horses, no follow-up information was available. Four horses were euthanased for reasons unrelated to the condition or its treatment. The horses over two years of age were in training or were being used for competitions in dressage or jumping or for breeding purposes, and in only one of them was an adventitious respiratory noise reported. All the horses up to two years of age were reported to be healthy.
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Bobbert, M. F., & Santamaria, S. (2005). Contribution of the forelimbs and hindlimbs of the horse to mechanical energy changes in jumping. J Exp Biol, 208(2), 249–260.
Abstract: The purpose of the present study was to gain more insight into the contribution of the forelimbs and hindlimbs of the horse to energy changes during the push-off for a jump. For this purpose, we collected kinematic data at 240 Hz from 23 5-year-old Warmbloods (average mass: 595 kg) performing free jumps over a 1.15 m high fence. From these data, we calculated the changes in mechanical energy and the changes in limb length and joint angles. The force carried by the forelimbs and the amount of energy stored was estimated from the distance between elbow and hoof, assuming that this part of the leg behaved as a linear spring. During the forelimb push, the total energy first decreased by 3.2 J kg(-1) and then increased again by 4.2 J kg(-1) to the end of the forelimb push. At the end of the forelimb push, the kinetic energy due to horizontal velocity of the centre of mass was 1.6 J kg(-1) less than at the start, while the effective energy (energy contributing to jump height) was 2.3 J kg(-1) greater. It was investigated to what extent these changes could involve passive spring-like behaviour of the forelimbs. The amount of energy stored and re-utilized in the distal tendons during the forelimb push was estimated to be on average 0.4 J kg(-1) in the trailing forelimb and 0.23 J kg(-1) in the leading forelimb. This means that a considerable amount of energy was first dissipated and subsequently regenerated by muscles, with triceps brachii probably being the most important contributor. During the hindlimb push, the muscles of the leg were primarily producing energy. The total increase in energy was 2.5 J kg(-1) and the peak power output amounted to 71 W kg(-1).
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Boden, L. A., Anderson, G. A., Charles, J. A., Morgan, K. L., Morton, J. M., Parkin, T. D. H., et al. (2006). Risk of fatality and causes of death of Thoroughbred horses associated with racing in Victoria, Australia: 1989-2004. Equine Vet J, 38(4), 312–318.
Abstract: REASONS FOR PERFORMING STUDY: Determining the risk of fatality of Thoroughbred horses while racing is essential to assess the impact of intervention measures designed to minimise such fatalities. OBJECTIVES: To measure the risk of racehorse fatality in jump and flat starts on racecourses in Victoria, Australia, over a 15 year period and to determine proportional mortality rates for specific causes of death. METHODS: All fatalities of Thoroughbred horses that occurred during or within 24 h of a race were identified from a database. The risk of a start resulting in a racehorse fatality in all races and within flat and jump races, proportional mortality rates, population attributable risk, population attributable fraction and risk ratios were calculated along with 95% confidence intervals. Poisson regression was also performed to estimate risk ratios. RESULTS: There were 514 fatalities over the 15 year period; 316 in flat races and 198 in jump races. The risk of fatality was 0.44 per 1000 flat starts and 8.3 per 1000 jump starts (18.9 x greater). The risk of fatality on city tracks was 1.1 per 1000 starts whereas on country tracks it was 0.57 per 1000 starts. Of the 316 fatalities in flat races, 73.4% were due to limb injury, 2.5% to cranial or vertebral injury and 19.0% were sudden deaths. Of the 198 fatalities in jump races, 68.7% were due to limb injury, 16.2% to cranial or vertebral injury and 3.5% were sudden deaths. The risk of fatality in flat starts increased between 1989 and 2004 but the risk in jump starts remained unchanged over the 15 year period. CONCLUSIONS: The risk of fatality in flat starts was lower in Victoria than North America and the UK but the risk in jump starts was greater. Catastrophic limb injury was the major reason for racehorse fatality in Victoria but there was a larger percentage of sudden deaths than has been reported overseas. The risk of fatality in jump starts remained constant over the study period despite jump racing reviews that recommended changes to hurdle and steeple races to improve safety. POTENTIAL RELEVANCE: This study provides important benchmarks for the racing industry to monitor racetrack fatalities and evaluate intervention strategies.
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Boissevain, I. (2007). [Animal and human rights in installments] (Vol. 132).
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Boray, J. C. (1969). Experimental fascioliasis in Australia. Adv Parasitol, 7, 95–210.
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Bottoms, G. D., Roesel, O. F., Rausch, F. D., & Akins, E. L. (1972). Circadian variation in plasma cortisol and corticosterone in pigs and mares. Am J Vet Res, 33(4), 785–790.
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Bourdin, P., & Laurent, A. (1974). [Ecology of African horsesickness]. Rev Elev Med Vet Pays Trop, 27(2), 163–168.
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